Our findings from completed qualitative light (LM) and electron (EM) microscopic studies, and from studies of anterograde axonal transport of radiolabelled proteins provide a strong indication that some retinal ganglion cells and their proximal nerve stumps are still morphologically and functionally intact as late as 28 days following optic nerve crush lesions, and also suggest that the substrate for axonal regeneration exists. We propose here to complete a qualitative and quantitative description of the basic morphology of axons and glia within the proximal portions of the optic nerve at varying times after crush lesions are made by using LM and EM methods. This information will be invaluable for determining the site along the nerve and the postoperative time at which maximal populations of near normal axons and optimal glial cell populations are available for application of experimental manipulations of axonal regrowth. We also propose to describe with LM and EM methods the changes in cell body size and cytoplasmic constituents in retinal ganglion cells at varying times after optic nerve lesions are made. The latter studies will provide information on how closely the morphological state of the ganglion cell bodies and their glial relations approximate the normal state, and will also give an indication of the protein synthetic activity of these cells at various times post-axotomy. This information is crucial to future experimental attempts to stimulate axonal growth through accelerating synthesis of structural proteins within axotomized cell bodies. In the third experiment we propose to determine when, or if, changes in retrograde axonal transport of horseradish peroxidase occurs after crushing the optic nerve. Correlation of results from these studies with results from previously described morphological studies of the axonal, cell body and glial response to axotomy will yield information on the relationship of retrograde transport mechanisms to the morphological state of damaged central neurons, and may provide an indication of whether or not the axon can signal the cell body that it has been damaged. If trophic substances are to be applied at, or near, the lesion site in future experiments, it is critical to know if these agents can be tansported retrogradely to the cell body where they may stimulate the cellular machinery which regulates axonal growth.